ASAHI Medical College at Okayama

Okayama-shi, Japan

ASAHI Medical College at Okayama

Okayama-shi, Japan

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Terayama R.,Okayama University of Science | Terayama R.,Okayama University | Maruhama K.,Okayama University of Science | Maruhama K.,Okayama University | And 8 more authors.
Archives of Oral Biology | Year: 2014

Objective To develop an objective method for assessing nociceptive behaviour in an animal model of capsaicin-induced intraoral pain. Changes in nociceptive responses were also examined after injury to the inferior alveolar nerve (IAN). Design Nociceptive responses evoked by the intraoral application of various doses of capsaicin were analyzed in lightly anaesthetized rats. The number of c-Fos protein-like immunoreactive (Fos-LI) neurons in the medullary dorsal horn (MDH) induced by the intraoral application of capsaicin was measured. Behavioural and c-Fos responses were also examined 14 days after injury to the IAN. Results Larger doses of intraoral capsaicin (1, 10 and 100 μg) induced vigorous licking behaviour and c-Fos response in the MDH in a reproducible manner. The magnitudes of both behavioural activity and the c-Fos response from the 10 and 100 μg doses of capsaicin were significantly greater than that by the 1 μg dose. Injury to the IAN exaggerated the behavioural and c-Fos responses evoked by intraoral capsaicin. Conclusions The intraoral application of capsaicin is a valid and reliable method for studying intraoral pain and hyperalgesia following nerve injury. © 2014 Elsevier Ltd.


Terayama R.,Okayama University of Science | Terayama R.,Okayama University | Kishimoto N.,Okayama University of Science | Yamamoto Y.,Okayama University of Science | And 10 more authors.
Neurochemical Research | Year: 2015

The number of c-Fos protein-like immunoreactive (c-Fos-IR) neurons in the spinal dorsal horn evoked by noxious stimulation was previously shown to be increased following peripheral nerve injury, and this increase was proposed to reflect the neuropathic pain state. The aim of this study was to investigate whether anomalous convergent primary afferent input to spinal dorsal horn neurons contributed to nerve injury-induced c-Fos hyperinducibility. Double immunofluorescence labeling for c-Fos and phosphorylated extracellular signal-regulated kinase (p-ERK) was performed to detect convergent synaptic input from different branches of the sciatic nerve after injury to the tibial nerve. c-Fos expression and the phosphorylation of ERK were induced by noxious heat stimulation of the hindpaw and also by electrical stimulation (ES) of the injured tibial nerve, respectively. The number of c-Fos-IR neurons was significantly decreased 3 days after the injury. However, the number of c-Fos-IR neurons returned to the control level 14 days after the injury. P-ERK immunoreactive (p-ERK-IR) neurons were induced in the central terminal field of the tibial nerve by ES of the tibial nerve. The topographic distribution pattern and number of such p-ERK-IR neurons remained unchanged after the nerve injury. The time course of changes in the number of double-labeled neurons, that presumably received convergent primary afferent input, showed a pattern similar to that of c-Fos-IR neurons after the injury. These results indicate that convergent primary nociceptive input through neighboring intact nerves may contribute to c-Fos hyperinducibility in the spinal dorsal horn. © 2014, Springer Science+Business Media New York.


Tomofuji T.,Okayama University of Science | Ekuni D.,Okayama University of Science | Irie K.,Okayama University of Science | Azuma T.,Okayama University of Science | And 5 more authors.
Biomedical Research | Year: 2011

Gingival response to periodontal inflammation generates excessive lipid peroxide and such a condition may augment systemic health through increased circulating lipid peroxide. The purpose of the present study was to investigate whether the generation of lipid peroxide in periodontal inflammation could induce tissue injury in the liver, heart, kidney and brain using a rat model. Twelve Wistar rats (8 week-old male) were divided into 2 groups: the periodontal inflammation group, receiving topical application of lipopolysaccharide and proteases to the gingival sulcus for 4 weeks, and the control group using instead pyrogen-free water. After blood samples were collected, specimens from the brain, heart, liver and kidney were resected to determine the concentration of 8-hydroxydeoxyguanosine (an indicator of oxidative DNA damage). Gingival and serum levels for hexanoyl-lysine were measured to evaluate lipid peroxide. Administration of lipopolysaccharide and proteases induced periodontal inflammation, with increasing gingival and serum levels of hexanoyl- lysine. The level of 8-hydroxydeoxyguanosine increased 2.27, 2.01, 1.49 and 1.40 times in mitochondrial DNA from the liver, heart, kidney and brain of rats with periodontal inflammation, respectively. The results reveal that excessive production of lipid peroxide following periodontal inflammation is involved in oxidative DNA damage of the brain, heart, liver and kidney.


Terayama R.,Okayama University of Science | Terayama R.,Okayama University | Tsuchiya H.,Okayama University of Science | Tsuchiya H.,ASAHI Medical College at Okayama | And 9 more authors.
Cellular and Molecular Neurobiology | Year: 2015

Previous studies demonstrated that the number of c-Fos protein-like immunoreactive (c-Fos-IR) neurons in the medullary dorsal horn (MDH) evoked by noxious stimulation was increased after peripheral nerve injury, and such increase has been proposed to reflect the development of neuropathic pain state. The aim of this study was to examine the MDH for convergent collateral primary afferent input to second order neurons deafferented by peripheral nerve injury, and to explore a possibility of its contribution to the c-Fos hyperinducibility. Double immunofluorescence labeling for c-Fos and phosphorylated extracellular signal-regulated kinase (p-ERK) was performed to detect convergent synaptic input. c-Fos expression and the phosphorylation of ERK were induced by the intraoral application of capsaicin and by electrical stimulation of the inferior alveolar nerve (IAN), respectively. The number of c-Fos-IR neurons in the MDH induced by the intraoral application of capsaicin was increased after IAN injury, whereas the number of p-ERK immunoreactive neurons remained unchanged. The number of double-labeled neurons, that presumably received convergent primary afferent input from the lingual nerve and the IAN, was significantly increased after IAN injury. These results indicated that convergent primary nociceptive input through neighboring intact nerves may contribute to the c-Fos hyperinducibility in the MDH and the pathogenesis of neuropathic pain following trigeminal nerve injury. © 2014, Springer Science+Business Media New York.

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